Abstract

Hyaloperonospora arabidopsidis is an obligate biotrophic oomycete shown to cause
downy mildew in Arabidopsis thaliana. The main focus of this project is examining
plant stress response and the strategies employed by H. arabidopsidis to infect
Arabidopsis and evade plant stress responses. Two regions of the H. arabidopsidis
genome containing genes expressed in planta during infection were bioinformatically
annotated. The results indicated the genes were involved in regulatory processes
associated with the pathogenicity of H. arabidopsidis but not a direct role in
pathogenicity. H. arabidopsidis infects its host by secreting effector proteins into the
cytoplasm and apoplastic space of the host. The secretome of H. arabidopsidis was
analysed to identify classes of cysteine rich apoplastic effectors. This identified 15
candidate elicitin (ELI) and elicitin-like (ELL) sequences, three Kazal-like serine
protease inhibitors and four candidates similar to the protein sequences of Ppats 14
and 24, expressed during infection.
A second set of aims was to identify potential signalling networks up activated
during plant defence responses to infection by H. arabidopsidis using a new model
developed by Beal et al (Beal, Falciani et al. 2005) to eventually engineer
transcriptional networks. Unfortunately this failed due to problems with the
experiment. However, it was still possible to identify signalling networks from a
second microarray time course experimental data set centred on signalling networks
up regulated in response to the onset of senescence, as they share overlapping
signalling pathways. The modelling methodology was used to model the
anthocyanin biosynthesis pathway. The model predicted the presence of AtMYB15
as a positive regulator of anthocyanin biosynthesis along with AtMYB90. Research
carried out by Nichola Warner (Warner 2008) suggested that AtMYB90 was not
essential for anthocyanin biosynthesis during senescence based on by comparing the
phenotype of the MYB90 knock out, IM28, with the wild type (WT) Col-0 using a
time course microarray. Models of networks of transcriptional regulation of the
anthocyanin biosynthesis pathway for IM28 and WT implicate AtMYB29 as a
positive regulator of anthocyanin biosynthesis.